Fig. 4

SCD maintains fatty acid desaturation to support viability of cancer cells. a DU145 cells were treated with SCD inhibitors (100 nM) or solvent (DMSO) for 48 h in medium with low serum or supplemented with BSA or BSA-coupled oleic acid (BSA-oleate). Quantitative lipid profiling of free fatty acids (FFA) content was performed by LC-MS/MS. Concentrations of saturated, mono-unsaturated and poly-unsaturated FFA are displayed. Data represent the mean ± SEM of three biologically independent replicates. Statistical comparisons were performed using Student t test (*p ≤ 0.05). b DU145 cells were treated with increasing concentrations of SCD inhibitor for 72 h in medium containing full (FS) or low serum (LS) or medium supplemented with BSA or BSA-oleate. Cell numbers are normalised to solvent treated controls. Statistical comparisons were performed using Student t test (*p ≤ 0.05). c DU145 cells were transfected with siRNA targeting SCD (siSCD), PLK1 (siPLK1) or non-targeting controls (siCtrl). Cells were cultured for 72 h in medium containing full (FS) or low serum (LS) or medium supplemented with BSA or BSA-oleate. Cell numbers are displayed relative to untreated siCtrl transfected cells. Data represent the mean ± SEM of two biologically independent experiments with two replicates each. Statistical comparisons were performed using Student t test (*p ≤ 0.05). d DU145, PC3 and MDA-MB-468 cells were treated with SCD inhibitor (SCDi I) or solvent (DMSO) under full (FS) or low (LS) serum conditions for 10 days. Cells were stained using crystal violet and quantified. Data represent mean ± SEM of two biologically independent experiments. Statistical comparisons were performed using Student t test (*p ≤ 0.05)